| Project/Area Number |
23790317
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General medical chemistry
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| Research Institution | Hokkaido University |
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Principal Investigator |
FUJIKURA DAISUKE 北海道大学, 人獣共通感染症リサーチセンター, 博士研究員 (70547794)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | death receptor 6 / DR6 / T細胞 / B細胞 |
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| Research Abstract |
Peripheral lymphocytes regulate the activation of immune network for protecting host homeostasis against an infection with several pathogens and tumor progressions, and an abnormality on the regulation causes auto-immunological diseases. Recently, it was demonstrated that Death receptor 6 (DR6) had an important role for a regulation of peripheral lymphocyte activation in response to antigen challenge. However, detail of molecular mechanism on a regulation for DR6's function, such as a specific ligand remains unclear. We identified a membrane protein specifically binding with DR6 (DR6L). In addition, in vitro binding assay showed that DR6L could specifically interact with DR6 than other members of TNFR family. Importantly, In vitro co-culture assay showed that DR6L expressed on an antigen presenting cell reduced an antigen dependent activation of T lymphocyte. These findings suggest that the identified protein, DR6L should act as a specific stimulator for DR6 in T cell activation.
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